Chronic immune thrombocytopenic purpura (ITP) is an autoimmune disorder characterized by thrombocytopenia due to the production of antiplatelet autoantibodies which result in platelet destruction by the reticuloendothelial system or inhibition of platelet production (McMillan, N. Engl. J. Med., 304:1135-1147, 1981; Kelton et al., Semin. Thromb. Haemost., 8:83-104, 1982). Autoantibody from approximately three-fourths of these patients is known to react with the membrane glycoprotein (GP) complexes --GPIIb/IIIa or GPIb/IX (van Leeuwen et al., Blood, 59:23-26, 1982; Woods et al., Blood, 63:368-375, 1984; Woods et al., Blood, 64:156-160, 1984; Beardsley et al., J. Clin. Invest., 74:1701-1707, 1984; McMillan et al., Blood, 70:1040-1045, 1987); of these, some have been shown to bind to GPIIIa (Beardsley et al., J. Clin. Invest., 74:1701-1707, 1984). However, little information is available on the precise location of epitopes on GPIIIa. A recent abstract by Kekomaki et al. showed that plasma from one ITP patient, which reacted with GPIIIa by immunoblotting, bound to a 60,000 dalton GPIIIa fragment resulting from chymotrypsin digestion (Kekomaki et al., Blood, 74:91, 1989).